Modulation of inflammation by chondroitin sulfate.

Abstract:

OBJECTIVE AND METHODS:To evaluate the immune-modulator effect of chondroitin sulfate (CS) by means of the review of the literature. RESULTS:Inflammatory reactions are primarily originated by infectious agents, immune reactions and by sterile tissue lesions that activate membrane receptors by means of pathogen-associated molecular patterns, tissue breakdown products and cytokines. The activation of membrane receptors triggers the phosphorylation of mitogen activated protein kinases and of the nuclear factor kappaB (NF-kappaB). The binding of NF-kappaB to the promoter of target genes enhances the expression of pro-inflammatory cytokines, inducible nitric oxide synthase, cyclooxygenase 2, phospholipase A2, and matrix metalloproteases, proteins that contribute to tissue damage and to the inflammatory reaction. The activation of NF-kappaB has a key role in the immune homeostasis and the inflammatory response and therefore, in the pathogenesis of numerous diseases. Chondroitin sulfate (CS) is able to diminish NF-kappaB activation and nuclear translocation in chondrocytes and synovial membrane, effects that may explain the benefits of CS in osteoarthritis. In addition, systemic CS reduces NF-kappaB nuclear translocation in macrophages and hepatocytes, raising the hypothesis that CS might be of benefit to treat other diseases with a strong inflammatory component. There is preliminary evidence in humans that CS improves moderate to severe psoriasis. Moreover, experimental and clinical data suggest that CS might be a useful therapeutic agent in diseases such as inflammatory bowel diseases, atherosclerosis, Parkinson's and Alzheimer's diseases, multiple sclerosis, amyotrophic lateral sclerosis, rheumatoid arthritis and systemic lupus erythematosus. DISCUSSION:These results urge for double blinded placebo-controlled trials to confirm the utility of CS in diseases with immune and inflammatory components.

authors

Vallières M,du Souich P

doi

10.1016/j.joca.2010.02.017

subject

Has Abstract

pub_date

2010-06-01 00:00:00

pages

S1-6

eissn

1063-4584

issn

1522-9653

pii

S1063-4584(10)00088-9

journal_volume

18 Suppl 1

pub_type

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